The effective treatment of fractures depends upon good softtissue
management. Fractures with a soft-tissue injury must be considered as surgical
emergencies. They need a sophisticated management protocol and an excellent
grading system to achieve the goal of uncomplicated healing with complete
restitution of function.

Open fractures and fractures with severe, closed soft-tissue damage are
often associated with polytrauma. Life-saving treatment must always take
priority and the surgeon must consider both the local injury and the whole
patient. Evaluation of the fracture must determine the extent of the softtissue
injury, which will be a key factor in management. The surgeon needs to be
familiar with the pathophysiology of a soft-tissue injury and the timing,
risks, and benefits of the different treatment options.

Pathophysiology and biomechanics

The condition of the wound after injury is determined by the following
factors:

type of insult and area of contact (blunt, penetrating, crushed, etc);

force applied;

direction of force;

area(s) of body affected;

wound contamination;

general physical condition of the patient.

A combination of these factors will produce different types of wounds.

Types of wounds.

Type of force

Type of injury

Sharp, pointed

Stab wound

Blunt

Contusion injury, cut

Extension, twist

Laceration

Shear

Degloving, wound defect, avulsions, abrasion

Combination of forces

Wounds from blows, impaling, bites, and gunshot

Crushing

Traumatic amputation, rupture, crush injury

Thermal

Burns

Wounds do not only differ in their shape, but also in the type of treatment
required and the prognosis for healing [1]. All injuries cause bleeding and
tissue destruction. This activates humoral and cellular mechanisms to stop
bleeding and resist infection. The sequential healing process starts
immediately after trauma and can be divided into three phases:

exudative or inflammatory phase;

proliferative phase;

reparative phase.

Pathophysiological responses in healing

Inflammatory phase

In the inflammatory phase, there is a massively increased interaction
between leukocytes and the injured microvascular endothelium. Trauma exposes
subendothelial collagen structures, leading to the aggregation of thrombocytes.
These release serotonin, adrenaline, and thromboxane-A, causing
vasoconstriction and producing cytokines such as platelet derived growth factor
(PDGF) and transforming growth factor (TGF-β) that have a strong chemotactic
and mitogenic effect on macrophages, polymorphonuclear neutrophils,
lymphocytes, and fibroblasts. Vasoconstriction and thrombocyte aggregation
contribute to the clotting and are an important part of the coagulation process
to stop bleeding. As a side effect the damaged tissue is underperfused, leading
to hypoxia and acidosis. The first cells to move from the small vessels into
the damaged tissue are polymorphonuclear neutrophils (PMN) and macrophages. PMN
are mobilized rapidly and produce an extremely vigorous initial response. The
main function of the macrophages is the removal of necrotic tissue and
microorganisms (phagocytosis and secretion of proteases) and the production and
secretion of cytokines (PDGF: mitogenic and chemotactic; TNF-α: proinflammatory
and angiogenic; β-FGF, EGF, PDGF, and TGF-β: mitogenic [2]).

Macrophages are responsible for the cytokine-induced early activation of
immunocompetent cells, the inhibition and destruction of bacteria, and the
removal of cell debris from the damaged tissue. However, the capacity of the
macrophages for phagocytosis is limited. If their capacity is overloaded by an
excessive amount of necrotic tissue, this will decrease the antimicrobial
activities of the mononuclear phagocytes. Since these phagocytic activities are
associated with superoxide production and high oxygen consumption, areas of
hypoxia and avascular areas are especially threatened by infection. Thus, the
pathophysiological rationale for performing radical surgical debridement of
dead tissue is to support the phagocytic process of the macrophages [3, 4].

Chemotactic substances, such as kallikrein, improve vascular permeability
and exudation by releasing the nanopeptide bradykinin that belongs to the
α2-globulin fraction. Prostaglandins, originating from tissue
debris, stimulate the release of histamine from mast cells and cause local
hyperemia, which is necessary for the metabolic processes of wound healing. In
addition, highly reactive oxygen and hydroxyl radicals are released during the
peroxidation of membrane lipids [5], which cause a further destabilization of
the cell membranes. These mechanisms result in an impairment of capillary
endothelial permeability, which again promotes hypoxia and acidosis in the
damaged areas. The infiltrating granulocytes and macrophages with their
capacity to resist infection and to engulf cell debris and bacteria
(physiological wound debridement) play a key role in the inflammatory response
of traumatized tissue and therefore have a decisive effect on the subsequent
reparative processes [5].

Proliferative and reparative phases

The proliferative phase begins when fibroblasts, followed by endothelial
cells, migrate into the area of the wound and proliferate there. This is
stimulated by mitogenic growth factors. These cells have a series of growth
factor receptors on their surfaces and, by paracrine and autocrine processes,
release several cytokines and synthesize the structural proteins of the
extracellular matrix (collagen). Fibronectins—proteins detached from the
surface of the fibroblasts by hydrolases—facilitate the bonding of type I
collagen to α1-chains. This is an important prerequisite for
progressive, reparative cell proliferation.

There is a smooth transition to the reparative phase and, simultaneously,
the proliferating endothelial cells form ingrowing capillaries, the typical
characteristic of granulation tissue. At the end of the reparative phase, water
content is reduced and the collagen initially formed is replaced by crosslinked
collagen type III. Fibrosis and scarring follow. The role of the growth factors
in scar formation remains unclear, but it seems that TGF-β plays a decisive
role [6, 7].

Problems of diagnosis and assessment

In open soft-tissue injuries, contamination and infection of the wound have
a negative effect on the healing process. In closed injuries, the degree of
injury and ischemic tissue may not be apparent and this can make diagnosis and
therapeutic decisions difficult [8]. Many modern imaging techniques permit
qualitative assessment of closed soft-tissue injuries, but clinically useful
quantitative assessment of damage is not yet available. Unfortunately, there
are no diagnostic criteria that allow definitive, preoperative differentiation
between reversibly (living) and irreversibly (dead) damaged tissue. Thus,
clinical experience and good judgment remains essential when selecting options
for treatment and prognosis. Drugs that can reduce posttraumatic microvascular
dysfunction and restore disturbed microcirculation may be available in the
future, and there is some experimental evidence that selective COX-2 inhibitors
[9] or N-acetylcysteine may be helpful [10].

Secondary damage mechanisms

Pathophysiology of soft-tissue injury

The immune response to trauma results in a drastic increase in
leukocyte-endothelial interaction and subsequent loss of endothelial integrity
with increased microvascular permeability.This leads to transendothelial
leakage of plasma and interstitial edema [11]. Edema may reduce the
microvascular blood supply in adjacent areas and this can result in progressive
necrosis of skeletal muscle in marginal areas that were not directly affected
by trauma. Thus, secondary tissue loss will occur.

Compartment syndrome

Compartment syndrome is due to raised pressure in a closed fascial or
osteofascial space that results in local tissue ischemia. This will compromise
neuromuscular function [12–14].

Mechanism and local pathology

Compartment syndrome is due to a vicious circle.

In closed fractures with soft-tissue injury, the threat posed by compartment
syndrome is not to be underestimated. It is triggered by an increase in
intramuscular pressure within a closed osteofascial space, at a level above a
critical microvascular perfusion pressure [15]. The cause may be exogenous
pressure (eg, restrictive plaster casts) or endogenous, due to an increase in
volume within the compartment from hemorrhage, perivascular infusions or edema
from abnormal capillary permeability caused by prolonged ischemia or
reperfusion. If impairment of the microcirculation from increased tissue
pressure persists, severe and irreversible neuromuscular dysfunction due to
hypoxia will result and lead to muscle necrosis and axonotmesis.

Originally, it was believed that the threshold for compartment syndrome was
a constant intramuscular pressure > 30 mm Hg. However, it is now recognized
that the key factor is the difference between the diastolic blood pressure
(dBP) and the intramuscular pressure (IMP). This determines the mean muscle
perfusion pressure (MPP):

Muscle perfusion
pressure

=

Diastolic blood
pressure

-

Intramuscular
pressure

If the muscle perfusion pressure is less than 30 mm Hg, there will be
hypoxia and anaerobic cell metabolism. It is important to note that blood
pressure has a direct relationship to perfusion pressure. Thus, multiply
injured patients with hypotension and hypoxia are predisposed to compartment
syndrome. Other injuries carrying a high risk of developing compartment
syndrome include: vascular injuries with peripheral ischemia, high-energy
trauma, severe soft-tissue crush, and comminuted fractures of the tibia [16].
The aim of any therapeutic procedure must be immediate compartment
decompression by dermatofasciotomy to achieve reperfusion of the capillary
bed.

Clinical manifestation

A compartment is an anatomical space, bounded on all sides by bone or deep
fascia, which contains one or more muscle belly. In addition, the surrounding
epimysium, the skin, or a constricting dressing can create such an envelope
with limiting boundaries. The relative inelasticity of the enveloping wall
means that if the muscle tissue swells, the pressure in the osseofascial
envelope will increase.

The diagnosis of a compartment syndrome in a conscious patient is usually
made by the clinical manifestation of unrelenting ischemic muscle pain that is
unrelieved by the expected amounts of analgesia. Any nerve traversing the
involved compartment will become ischemic, often causing numbness and tingling
in the nerve distribution. Reporting of these symptoms requires an alert,
conscious and cooperative patient whose perceptions or response have not been
changed by distracting injury, alcohol, or drugs.

Clinical examination will show a tense, swollen compartment; palpation will
reproduce the pain and passive stretching of the digital muscles of the
involved compartment will also increase the pain. This sign may be helpful,
although not very specific. A sensory deficit in the nerve traversing the
compartment may or may not be present. Motoric weakness is a late change.
Pulses are always palpable in a compartment syndrome, because in a normotensive
patient the muscle pressure rarely exceeds the systolic level. Persistent,
unexplained tachycardia should also be regarded as a possible sign of
compartment syndrome in the unconscious patient once other causes (eg,
hypovolemia) have been excluded.

Tissue necrosis will result when interstitial pressure is increased beyond
an individual threshold for a long enough period of time. Patients who suffer
an untreated or overlooked compartment syndrome will develop ischemic
contracture, as described by Volkmann. This results in a contracted,
nonfunctional limb. The surgeon must be aware that all limb injuries are at
risk of compartment syndrome. It is most common in high-energy fractures and
crush injuries but can also be seen after simple injuries and without any
associated fracture. Patients on anticoagulant therapy are at high risk and
young males have a higher risk of compartment syndrome, possibly because they
have relatively thick and inelastic fascia. Compartment syndrome can also
develop after reperfusion of an ischemic limb. This is seen in patients who
have been unconscious for a number of hours (eg, drug addicts) and also after
repair of arterial injuries. Therefore, most trauma patients who have an
arterial repair must have prophylactic distal dermatofasciotomies.

Diagnosis

Differential diagnosis includes arterial injury and peripheral nerve injury:
Absent pulses indicate arterial injury; peripheral nerve injury is the
diagnosis of exclusion. A high amount of suspicion is essential if cases of
compartment syndrome are not to be missed. The surgeon must be vigilant as the
symptoms and signs may be minimal. Medical and nursing staff must be aware that
analgesics can mask the symptoms and this can be a particular problem following
surgery when patient controlled analgesia (PCA) is administered. Excessive use
of the PCA should alert staff to the possibility of compartment syndrome.

Compartment syndrome can also be diagnosed by tissuepressure measurements.
This is extremely helpful in situations where clinical examination is
unreliable, such as in head injury or intoxicated patients. The tissue pressure
is usually elevated before signs and symptoms develop and so pressure
measurements can be used to diagnose an impending compartment syndrome. They
can also be used to monitor patients at high risk of developing this
complication following surgery. Pressure measurements can be taken by a variety
of techniques. The infusion technique is simple and continuous, but may worsen
the syndrome and usually has a higher pressure threshold than other methods.
The wick technique uses some fine material inside the catheter to maintain the
opening to allow continuous monitoring. The stick technique is usually a
reliable, simple system to use but the appropriate equipment must be purchased.
Over the past few years, fine-wire, intracompartment pressure transducers have
become available. These are simple and reliable and allow continuous pressure
monitoring in the perioperative period [17].

Management

The initial treatment should include release of all circumferential
dressings and elevation of the limb to the level of the heart (to maximize
tissue perfusion pressure).

Compartment syndrome is a surgical emergency and the treatment of choice
is immediate dermatofasciotomy.

In trauma, percutaneous fasciotomy is not indicated since the skin, as
long as it remains intact, acts as a limiting membrane and may sustain the
compartment syndrome.

Compartment syndrome is most common in the lower leg. All four compartments
must be released using either Mubarak’s double-incision technique [18] or the
parafibular dermatofasciotomy described by Matsen [12]. The fibulectomy-
fasciotomy, as popularized in the vascular surgical literature, is
contraindicated for trauma patients. Even if the pressure is increased in only
one or two compartments, it is mandatory to completely release all. This is
true for every possible location of compartment syndrome in the upper or lower
extremity.

Severe soft-tissue injury results in local microvascular and cellular damage
and can also lead to a marked systemic inflammatory response due to the release
of proinflammatory cytokines (TNF-α, IL-1, IL-6, IL-10). These affect vascular
endothelia in various organs, resulting in margination, migration and
activation of polymorphonuclear neutrophils, increased capillary permeability,
interstitial edema and an inflammatory response. The systemic inflammatory
response syndrome (SIRS) results in damage to various organs—multiple organ
dysfunction syndrome (MODS). The damage is not only to organs such as the lungs
(ARDS), liver, gastrointestinal tract, kidneys, myocardium, and central nervous
system, but also affects the entire immune system: Sepsis remains the most
common cause of death in these patients [19–21]. Thus, the pathophysiological
changes in damaged tissue after soft-tissue trauma are the product of a vicious
circle.

Emergency evaluation of soft-tissue injury

Case history

To determine the appropriate choice and timing of treatment, the surgeon
needs to know when, where, and how the injury occurred. For instance, prolonged
entrapment in a car suggests the possibility of a compartment syndrome, and
barnyard accidents have a high risk of infection. Most important of all is the
knowledge of the amount and direction of force or energy causing the injury.
This determines both the extent of the injury and the necessary steps in
treatment. The greater the force, the more serious the damage and sequelae will
be.

Vascular status

It is mandatory to determine the vascular status of all injured limbs. The
peripheral pulses, temperature and capillary refill must be checked and
compared with the uninjured side. Although the absence of a palpable pulse is
an important pointer to potential vascular damage, the presence of a pulse or
good capillary refill does not necessarily guarantee an intact vascular supply.
Doppler examination of the injured and unharmed extremity may be helpful for
screening and the ankle-brachial index (ABI) is also useful [22]. In all cases
of doubt or where the case history, the physical examination, or the
radiographic fracture pattern suggests vascular damage, the opinion of a
vascular surgeon must be obtained urgently. Management strategies include
urgent angiography in the vascular radiology suite, immediate on-table
angiography or direct w of the injured vessel. The method chosen will depend
upon local facilities and protocols.

Neurological status

Neurological assessment can be difficult in unconscious patients with
multiple injuries. However, examination of the reflexes and the response to
strong, painful stimuli give some indication of major deficits. These
examinations have to be performed repeatedly because the confirmation of a
major nerve deficit can be decisive in the choice between salvage versus
amputation in severely injured extremities.

Soft-tissue conditions

Soft-tissue injuries in closed fractures are less obvious than in open
fractures, but still have enormous importance. Their evaluation can be much
more difficult than open fractures and their severity is easily underestimated.
Simple abrasions represent an injury of the physiological skin barrier and can
allow the development of deep infection. If this occurs, it is usually more
challenging and difficult to manage than a simple perforation of the skin.

In open fractures, the wound is covered by a sterile dressing at the site of
the accident and this should not be removed before the patient is in the
operating room. Only there, and under sterile conditions, the full extent of
the soft-tissue damage is assessed. (Some authors allow one removal for a
photograph to facilitate planning.)

The degree of wound contamination is important and influences the course and
outcome of the injury. Foreign bodies and dirt particles give useful
information about the level of contamination and help the surgeon with grading
these injuries. High-velocity shotgun wounds and farming accidents are
considered as severely contaminated.

After formal surgical skin preparation, with washout of dirt and debris, the
traumatic wound is excised and, if necessary, extended. Gentle manipulation and
inspection give best information about the condition of the bone and the extent
of softtissue damage. The surgical debridement becomes a diagnostic exercise as
skin edges, subcutaneous fat, muscles, and fascial elements are checked for
viability and bleeding. The definitive assessment of a soft-tissue injury
requires an experienced surgeon because it determines the treatment protocol as
well as the choice of implant for fracture fixation.

Compartment syndrome is seen most frequently in the lower leg but can also
occur in the forearm, buttock, thigh, hand, and foot. Compartment syndromes may
occur at any time during the first few days after trauma or surgery.

Assessment of the fracture

At the time of debridement, careful inspection of bone fragments, their
relationship to the soft-tissue envelope and blood supply, as well as the
information obtained from x-rays, help to optimize assessment of the damage.
The radiographic fracture pattern provides indirect information about the
softtissue injury, and can show foreign bodies, dirt, soft-tissue density, or
entrapped air around and/or distal to the fracture site.

Management algorithm

The following figure shows a flow chart of considerations and actions
required in the management of fractures with concomitant softtissue damage.

Management algorithm for the treatment of fractures with a concomitant
soft-tissue injury (modified according to Waydhas and Nast-Kolb).

Classification of soft-tissue injury in fractures

A classification of the soft-tissue injury should consider all essential
factors and guide treatment. It effectively decreases complications by
preventing avoidable treatment errors and should be of some prognostic value.
There is also the possibility to monitor and compare standardized treatment
protocols. The most commonly used classifications were devised by Gustilo and
Anderson [23, 24] and by Tscherne [25].

Gustilo classification of open fractures

Gustilo and Anderson developed their classification on the basis of a
retrospective and prospective analysis of 1,025 open fractures. They initially
described three types, but clinical application led Gustilo, Mendoza, and
Williams to extend and subdivide the classification of the severe (type III)
injuries into subgroups A, B, and C.

Type I: These are fractures with a clean wound of less than 1 cm in
size with little or no contamination. The wound results from an inside-out
perforation by one of the fracture ends. The fracture pattern is simple (eg,
spiral or short oblique fractures).

Type II: Skin laceration is longer than 1 cm but the surrounding
tissues have minor or no signs of contusion. There is no dead muscle present
and the fracture instability is moderate to severe.

Type III: There is extensive soft-tissue damage, frequently with
compromised vascularity with or without severe wound contamination. The
fracture pattern is complex with marked fracture instability.

Because of the many different factors occurring in this group, Gustilo
proposed three subtypes.

Type IIIA: It usually results from an high-energy trauma. There is
still adequate soft-tissue coverage of the fractured bone, despite extensive
soft-tissue laceration or flaps (similar to AO classification IO 2).

Type IIIB: There is extensive soft-tissue loss with periosteal
stripping and bone exposure. These injuries are usually associated with massive
contamination (similar to AO classification IO 3).

Type IIIC: This is associated with any open fracture associated with
arterial injury requiring repair. It is independent of the fracture type
(similar to AO classification IO 4)

Tscherne classification of open soft-tissue injuries

In Tscherne’s classification, soft-tissue injuries are grouped into four
categories according to severity. The fracture is labeled as open or closed by
an “O” or a “C”.

Open fracture grade I (Fr. O 1): The skin is lacerated by a bone
fragment from the inside. There is no or minimal contusion of the skin, and
these simple fractures are the result of indirect trauma (type A1 and A2
fractures according to the AO classification).

Open fracture grade II (Fr. O 2): There is a skin laceration with a
circumferential skin or soft-tissue contusion and moderate contamination. All
open fractures resulting from direct trauma (AO classification type A3, type B
and type C) are included in this group.

Open fracture grade III (Fr. O 3): There is extensive softtissue
damage, often with an additional major vessel and/ or nerve injury. Every open
fracture that is accompanied by ischemia and severe bone comminution belongs in
this group. Farming accidents, high-velocity gunshot wounds, and compartment
syndrome are included because of their high risk of infection.

Open fracture grade IV (Fr. O 4): These are subtotal and total
amputations. Subtotal amputations are defined by the Replantation Committee of
the International Society for Reconstructive Surgery as a “separation of all
important anatomical structures, especially the major vessels, with total
ischemia”. The remaining soft-tissue bridge may not exceed 1/4 of the
circumference of the limb.

Cases requiring revascularization can be classified as grade III or IV
open.

Tscherne classification of closed fractures

Closed fracture grade 0 (Fr. C 0): There is no or minor soft-tissue
injury with a simple fracture from indirect trauma. A typical example is the
spiral fracture of the tibia in a skiing injury.

Closed fracture grade I (Fr. C 1): There is superficial abrasion or
skin contusion, simple or medium severe fracture types. A typical injury is the
pronation-external rotation fracture dislocation of the ankle joint: The
soft-tissue damage occurs through fragment pressure at the medial
malleolus.

Closed fracture grade II (Fr. C 2): There are deep contaminated
abrasions and localized skin or muscle contusions resulting from direct trauma.
The imminent compartment syndrome also belongs to this group. The injury
results in transverse or complex fracture patterns. A typical example is the
segmental fracture of the tibia from a direct blow by a car fender.

Tscherne developed a soft-tissue classification because he realized that
closed injuries were frequently underestimated. From this original
classification evolved the much more elaborate Hanover fracture scale.

Many problems in the treatment of complex fractures are due to high-velocity
injury patterns causing severe soft-tissue damage. The above mentioned and most
frequently used classifications have shown limitations for these types of
injuries. Brumback [26] has shown that there is only a moderate interobserver
reliability in classifying open fractures using the Gustilo and Anderson
classification. For these reasons, Tscherne and Oestern [25] developed the
Hanover fracture Scale (HFS) from an analysis of approximately 1,000 open
fractures from 1980 to 1989 and this has been further updated and validated
[27, 28].

Hanover fracture scale with correlation of the fracture scale score to
Tscherne’s classification of open and closed fractures.

A Fracture type

Points

C Ischemia/compartment syndrome

Points

Type A

1

No

0

Type B

2

Incomplete

10

Type C

4

Complete

Bone loss

< 4 hours

15

< 2 cm

1

4-8 hours

20

> 2 cm

2

> 8 hours

25

B soft tissues

Points

D Nerves

Points

Skin (wound, contusion)

Palmar/plantar sensations

No

0

Yes

0

< 1/4
circumference

1

No

8

1/4-1/2

2

Finger/toe motion

1/2-3/4

3

Yes

0

> 3/4

4

No

8

Skin defect (loss)

No

0

E Contamination

Points

< 1/4
circumference

1

Foreign bodies

1/4-1/2

2

None

0

1/2-3/4

3

Single

1

> 3/4

4

Multiple

2

Deep soft tissues (muscle, tendon,
ligaments, joint capsule)

Massive

10

No

0

F Bacteriological smear

Points

< 1/4
circumference

1

Aerobe 1 germ

2

1/4-1/2

2

Aerobe > 1 germ

3

1/2-3/4

3

Anaerobe

2

> 3/4

6

Aerobe/anaerobe

4

Amputation

G Onset of treatment

Points

No

0

(Only if soft-tissue score >
2)

Subtotal/total
guillotine

20

6-12 hours

1

Subtotal/total crush

30

> 12 hours

3

Classification

Total A-B

Classification

Total C-G

Fr. O 1

2-3 points

Fr. C 0

1-3 points

Fr. O 2

4-19 points

Fr. C 1

4-6 points

Fr. O 3

20-69 points

Fr. C 2

7-12 points

Fr. O 4

> 70 points

Fr. C 3

> 12 points

The scale considers every detail of the injury to the involved extremity and
forms a checklist. The fracture type (according to the Müller AO
Classification), skin condition, underlying soft tissues, vascularity,
neurological status, level of contamination, presence or absence of compartment
syndrome, time interval between injury and treatment, and the overall severity
of the injury are summed to provide the total score. Bone loss represents bone
fragments that have been lost at the site of the accident. The longest axis of
the missing piece of bone is measured and graded either as smaller or greater
than 2 cm.

For the evaluation of soft tissues, the score provides three different
categories:

size of the skin wound;

area of skin loss;

damage to deep soft tissues such as muscles and tendons.

Due to different diameters and thickness at different levels in the involved
extremity, the extent of soft-tissue damage is related to the volume of the
soft-tissue envelope. The three different categories of soft-tissue damage
allow evaluation of both superficial and deep injury. The category Amputation
evaluates the mechanism of injury and the possibility of replantation. An exact
evaluation of the neurological status is often difficult at the time of
admission but monitoring of reflexes allows a gross estimation of possible
neurological damage. This can be important in the process of deciding for or
against limb salvage. At the time of admission, a bacteriological evaluation
may not yet be available. However, bacterial contamination is still a part of
the score to remind the treating surgeons to take it into account. The overall
score guides general patient management and local treatment. Some of the
category scores (eg, bone score or soft-tissue score) are valuable for
treatment decisions and estimation of possible complications [29].

The AO soft-tissue grading system

Because of the limitations of the existing classification systems, including
moderate interobserver reliability and the grading of many different injuries
into the same subgroup, AO developed a more detailed and precise grading system
for fractures with soft-tissue damage. This grading system identifies injuries
to the different anatomical structures and assigns them to different severity
groups. The skin (integument), muscles and tendons, and the neurovascular
system are the targeted anatomical structures; the fracture is classified
according to the AO classification of fractures. The grading of the skin lesion
is done separately for open or closed fractures: The letters “O” and “C”
designate these two categories. Each is divided into 5 severity groups. Thus,
IC 1 represents the injury of the integument in a closed fracture. The digit
“1” indicates the least severe injury. IC 5 has the most severe soft-tissue
damage.

Although there may be considerable damage to a muscle envelope, there is
rarely an injury to tendons except in severe injuries (Tab 1.6-5). The
involvement of the neurovascular system (Tab 1.6-6) always indicates a most
severe injury of the kind represented by the Gustilo types IIIB and IIIC and
has a high complication rate. Muscle and tendon injuries as well as
neurovascular injuries are of high prognostic value for the fate of the
extremity.

AO soft-tissue classification: muscle and tendon lesions (MT).

AO soft-tissue classification: nerve and vessel lesions (NV).

This system allows a comprehensive description of the entire injury complex.
The numbers and letters are useful for computerization, audit, and research. In
everyday clinical practice it is the use of accurately defined, descriptive
terms that aid good decision making and communication. For example, a simple,
closed spiral tibial midshaft fracture from skiing with no injury of skin,
muscles, tendons, nerves, or vessels is graded: 42-A1.2/IC1-MT1-NV1.

In contrast, the previous figures in the section "IO 5 extensive
degloving" show a Monteggia type elbow dislocation fracture with
extensive muscle and tendon injury but no neurovascular damage. This will be
graded as 22-B1/IO5- MT4-NV1. The figures in section "IO 4 considerable,
full-thickness contusion, abrasion, extensive open degloving, skin loss"
illustrate an open, complex, segmental tibial shaft fracture with an open wound
greater than 5 cm, muscle defect, and tendon laceration. There is no nerve
injury but an injury of the peroneal artery. This injury will be graded as
42-C2.3/IO4-MT4-NV3.

Usage of classification systems

Higher grades of the Gustilo classification of open fractures and of the
Tscherne classification of closed fractures are most challenging from the
therapeutic point of view. These injuries have the highest complication rates
and can cause severe disability of the patient. We should keep in mind that
classification systems have several objectives, namely to

facilitate communication;

assist decision making;

identify treatment options;

anticipate problems;

suggest treatment method;

predict the outcome;

enable comparison with similar cases;

assist documentation and audit.

Conclusion

The effective treatment of fractures depends upon good management of the
soft tissues. The surgeon must carefully evaluate the injury by systematically
examining each structure that could be damaged: the skin, subcutaneous tissue,
muscle and tendons, nerves, vessels, and bones. The possibility of compartment
syndrome should always be considered and it must be recognized that closed
injuries may be associated with as much soft-tissue damage as open injuries.
Careful evaluation will allow the surgeon to classify the fracture using one of
the comprehensive grading systems such as the AO system or the Hanover fracture
scale. This will guide decision making, allow clear communication, and give an
indication of potential complications and outcome.

[25] Tscherne H, Oestern HJ (1982) A new classification of
soft-tissue damage in open and closed fractures. Unfallheilkunde;
85(3):111–115.

[26] Brumback RJ, Jones AL (1994) Interobserver agreement in the
classification of open fractures of the tibia. The results of a survey of two
hundred and forty-fi ve orthopaedic surgeons. J Bone and Joint Am;
76(8):1162–1166.